Plate Nº 62 · recorded October 10, 2026
Biology & EvolutionReported finding
Newly discovered cell type helps shape heart blood vessel growth
On August 20, Weill Cornell researchers reported in Nature Communications a previously unknown perivascular cell in zebrafish that wraps coronary vessels and helps stop blood vessel growth after heart development or injury.
By James Calloway3 min read560 words
In brief
- Published August 20 in Nature Communications (DOI: 10.1038/s41467-026-77008-y)
- Led by Dr. Jingli Cao of Weill Cornell Medicine with Björn Perder and Dr. Yu Xia
- Identified a new perivascular cell type controlled by the master regulator gene scxa
- Low oxygen (hypoxia) activates scxa, steering epicardial progenitors toward the perivascular fate
- Humans carry the related gene SCX, which currently activates scar-forming cells after a heart attack
On August 20, researchers at Weill Cornell Medicine reported in Nature Communications a previously unknown cell type that helps control blood vessel growth in the zebrafish heart. The study identifies a perivascular cell that wraps coronary vessels and produces a collagen-based signal that stops vessel expansion once the network is large enough.
Lead author Dr. Jingli Cao, associate professor of cell and developmental biology at Weill Cornell and a member of its Cardiovascular Research Institute, said: "Our ultimate goal is to repair the damaged human heart. Being able to rebuild vessels at the right time and in the right location is key to the process."
What did the team actually discover?
Working with zebrafish, Cao and colleagues Björn Perder, a graduate student, and Dr. Yu Xia, a postdoctoral fellow, cataloged genes activated in epicardial progenitor cells after heart injury. The epicardium is the thin outer cell layer that covers the heart.
One gene stood out: scxa, a master regulator. It directs progenitor cells to become the new perivascular cells. These cells wrap around coronary blood vessels and release a small protein fragment derived from collagen. The fragment acts as a brake on vessel growth.
"During development or when the heart is damaged, you need to build the right amount of blood vessel — and you need to know when to stop," Cao said. "This system provides that layer of control."
How does the body switch the system on?
The new paper links this control to oxygen levels. Low oxygen, a condition called hypoxia, temporarily activates scxa. The signal steers a subset of epicardial progenitors toward the perivascular fate. The cells then surround coronary vessels and regulate their development and remodeling.
Earlier work from Cao's lab showed that hypoxia-related signals from the epicardium coordinate heart muscle and coronary vessel growth. The current study adds a specific molecular mechanism to that picture. Together, the results suggest low oxygen acts as an environmental cue, not just a stress signal.
Why study zebrafish hearts?
Zebrafish can regenerate heart tissue after injury. Human hearts typically form permanent scars after a heart attack. Understanding which cells and genes zebrafish rely on could point to targets for reactivating similar programs in people.
The researchers stress that humans carry a related gene, SCX. After a heart attack, however, mammalian SCX turns on in cardiac fibroblasts — cells that drive scar formation rather than regeneration.
"Maybe in the future we can use SCX to reactivate human epicardial cells and steer them toward generating the cells and signals that promote human heart regeneration," Cao said.
How far is the work from clinical use?
Cao's lab is now testing these ideas in cultured human epicardial cells and in cardiac organoids — miniature lab-grown heart tissue. The long-term aim is a "biological bandage" that delivers controlled muscle and vessel growth at an injury site. Such a tool could one day limit scar tissue and rebuild functional vasculature.
"I don't think there will be just one magic factor that controls regeneration," Cao said. "But we've discovered one more factor, one more mechanism that could eventually contribute to turning on epicardial cells and repairing human hearts."
The findings appear in Björn Perder et al, "Hypoxia-activated scleraxis a mediates epicardial progenitor differentiation into a unique cardiac perivascular cell type," Nature Communications (2026). DOI: 10.1038/s41467-026-77008-y.
via Medical Xpress (Source)
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